Yeast cells begin to develop heat resistance immediately after UV- or Alpha-irradiation, with maximal resistance reached 6-8 hours afterwards; bacteria begin synthesis of heat-stress proteins (hsp's) immediately after exposure to UV or to nalidixic acid. By contrast, insects develop significant resistance to heat (and to some other stresses) 2 weeks after -irradiation, and the resistance persists for many months; heat resistance develops promptly in heat-shocked insects, however, and declines within a few days. Slow development and long persistence of heat resistance in irradiated insects may stem from the fact that the critical sites of heat damage in intact insects are in differentiated postmitotic tissues; tight coiling of the chromatin in such tissues may alter the rate of recognition of, and the response to, DNA lesions. This phenomenon could greatly affect combined-modality treatment of cancer and, in particular, the response of differentiated normal tissues; fundamental aspects of cell regulation are also involved. Long-term objectives are comparisons between dormant vs. vegetative cells and between irradiation and heat shock in determining the magnitude and the kinetics of induction of heat resistance and of hsp synthesis. Chromatin is tighly coiled during the dry dormant stage of plant seeds, but "opens up" during preparation for germination after rehydration. Accordingly, irradiation or rapid or gradual heating will be applied to dry soybean (Gycine max) and barley (Hordeum vulgare) seeds, or at various times during or after rehydration. Subsequent heat stress will consist of a brief period at 52 degree or at 45 degree. In addition, the protection by a brief period of 45 degree against subsequent heating will be compared in normal and previously irradiated groups. End points scored will include fraction of seeds germinating, seedling growth, total protein synthesis, cell viability by dye exclusion, and hsp synthesis using electrophoresis.